2012 arrhythmia essentials

Arrhythmia
Essentials
Brian Olshansky, MD
Professor of Medicine, Cardiac Electrophysiology Section
Division of Cardiology
Department of Internal Medicine
University of Iowa Hospitals, Iowa City, IA

Mina K. Chung, MD
Associate Professor of Medicine
Cleveland Clinic Lerner College of Medicine of Case Western Reserve University
Cardiac Electrophysiology and Pacing
Department of Cardiovascular Medicine, Heart and Vascular Institute
Department of Molecular Cardiology, Lerner Research Institute
Cleveland Clinic, Cleveland, OH

Steven M. Pogwizd, MD
Featheringill Endowed Professor in Cardiac Arrhythmia Research
Professor of Medicine, Physiology & Biophysics, and Biomedical Engineering
Director, Center for Cardiovascular Biology
Associate Director, Cardiac Rhythm Management Laboratory
University of Alabama at Birmingham, Birmingham, AL

Nora Goldschlager, MD
Professor of Clinical Medicine
University of California, San Francisco
Chief, Clinical Cardiology
Director, Coronary Care Unit
ECG Laboratory and Pacemaker Clinic
San Francisco General Hospital, San Francisco, CA

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Library of Congress Cataloging-in-Publication Data
Arrhythmia essentials / Brian Olshansky . . . [et al.].
p. ; cm.
Includes bibliographical references and index.
ISBN 978-0-7637-7476-9
1. Arrhythmia. I. Olshansky, Brian.
[DNLM: 1. Arrhythmias, Cardiac. WG 330]
RC685.A65A7713 2012
616.1’28—dc22
2010038843
6048
Printed in the United States of America
15 14 13 12 11
10 9 8 7 6 5 4 3 2 1

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Table of Contents

iii

TABLE OF CONTENTS

PREFACE ....................................................... v
1. SINUS NODE—NORMAL AND
ABNORMAL RHYTHMS .......................... 1
Normal Sinus Node .................................... 2
Sinus Node Dysfunction, Including
Sinus Bradycardia and Tachy-Brady
Syndrome............................................... 6
Sinoatrial Exit Block.................................. 13
Sinus Pause/Arrest ................................... 18
Sinus Tachycardia .................................... 20
Postural Orthostatic Tachycardia
Syndrome............................................. 24
2. BRADYARRHYTHMIAS—CONDUCTION
SYSTEM ABNORMALITIES ................... 26
Atrioventricular Conduction
Abnormalities
First-Degree AV Block ........................... 27
Second-Degree AV Block—Mobitz
Type I................................................ 31
Second-Degree AV Block—Mobitz
Type II............................................... 35
Second-Degree AV Block—2:1 AV
Block ................................................. 40
High-Degree Advanced AV Block .......... 43
Third-Degree (Complete) AV Block ....... 47
Caveats ................................................ 52
Atrioventricular Dissociation ................. 54
Intraventricular Conduction
Abnormalities
Left Bundle Branch Block ...................... 56

Right Bundle Branch Block .................... 59
Rate-Related Bundle Branch
Block ................................................. 63
Fascicular Block .................................... 66
Unifascicular Block................................ 66
Bifascicular Block .................................. 70
Trifascicular Block ................................. 75
3. ECTOPIC COMPLEXES AND
RHYTHMS ............................................. 79
Premature Atrial Complexes..................... 80
Premature Junctional Complexes ............. 83
Premature Ventricular Complexes ............ 85
Escape Beats, Escape Rhythms, and
Accelerated Rhythms ............................ 95
Ectopic Atrial Rhythm .............................. 98

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Wandering Atrial Pacemaker ................... 99
Junctional Rhythm ................................. 101
Accelerated Idioventricular
Rhythm .............................................. 104
4. TACHYCARDIA .................................... 106
Tachycardia Mechanisms ....................... 107
Narrow QRS Complex Tachycardia ......... 108
Wide QRS Complex Tachycardia ............ 109
5. SUPRAVENTRICULAR
TACHYARRHYTHMIAS ....................... 115
Supraventricular Tachycardia ................. 116
Atrial Arrhythmias .................................. 116

Atrial Fibrillation..................................... 129
Atrial Flutter .......................................... 154
Atrioventricular Nodal Reentry
Tachycardia ........................................ 164
Junctional Tachycardia ........................... 171
Preexcitation Syndromes ........................ 173
6. VENTRICULAR
TACHYARRHYTHMIAS ....................... 186
Nonsustained Ventricular
Tachycardia ........................................ 187
Sustained Ventricular Tachycardia .......... 195
Ventricular Fibrillation ............................ 209
Specific Ventricular Arrhythmia
Syndromes ......................................... 213
Ventricular Tachyarrhythmias in the
Setting of Structural Heart
Disease............................................... 214
Ventricular Arrhythmias
Associated with Ischemic
Cardiomyopathy ........................ 214
Ventricular Arrhythmias
Associated with Nonischemic
Cardiomyopathy ........................ 214
Hypertrophic
Cardiomyopathy ........................ 215
Arrhythmogenic Right Ventricular
Cardiomyopathy ........................ 217
Ventricular Arrhythmias in Structurally
Normal Hearts .................................... 219
Outflow Tract

Ventricular Tachycardias ............ 219
Idiopathic Left Ventricular or
Fascicular Tachycardia ................ 221

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iv

Arrhythmia Essentials
Long QT Syndrome ....................... 221
Brugada Syndrome ........................ 224
Catecholaminergic Polymorphic
Ventricular Tachycardia .............. 227
Drug- and Metabolic-Induced
Torsades de Pointes ................... 230
Primary and Secondary Prevention
of Sudden Cardiac Death ................... 236

7. CARDIAC PACING AND
PACEMAKER RHYTHMS ..................... 240
Pacemaker Rhythms............................... 241
Indications for Pacing ............................ 258
8. IMPLANTABLE CARDIOVERTER
DEFIBRILLATORS ................................. 261
Implantable Cardioverter Defibrillators ... 262
Cardiac Resynchronization Therapy ........ 267
9. DRUG EFFECTS AND ELECTROLYTE
DISORDERS ......................................... 269
Drug Toxicity ......................................... 270

Digitalis Toxicity ..................................... 270
Electrolyte Disorders .............................. 275
Calcium Disorders .................................. 280

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10. ATHLETES AND ARRHYTHMIAS ....... 283
11. EVALUATION OF THE PATIENT
WITH SUSPECTED ARRHYTHMIAS ... 287
Outpatient Approach to Arrhythmia
Monitoring ....................................... 288
Carotid Sinus Massage......................... 289
Electrophysiology Studies..................... 290
Palpitations .......................................... 291
Syncope............................................... 294
12. TREATMENT OF
ARRHYTHMIAS .................................. 296
Pharmacologic Therapy for Clinical
Arrhythmias ..................................... 297
Antiarrhythmic Agents ..................... 297
Anticoagulant Drugs ........................ 309
Nonpharmacologic Therapy ................. 311
SUGGESTED READING ............................. 314
INDEX ........................................................ 317

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Preface

v

PREFACE

Arrhythmia Essentials is a comprehensive, yet practical handbook that provides an approach
to patients who have cardiac arrhythmias, including those arrhythmias that occur in specific
clinical settings. The book is meant to be used to help assess and manage patients with
virtually all arrhythmias and related symptoms and includes treatment strategies that may be
considered. To this end, we have focused on a step-by-step approach for ease of use. The
book is divided into chapters that include sinus node function, bradycardias, tachycardias,
heart block, normal and abnormal pacemaker and implantable defibrillator function, and special arrhythmia-related topics such as syncope, palpitations, arrhythmias in the athlete, and
other clinical conditions of importance. Provided also is a section that summarizes available
drugs useful to treat patients with cardiac arrhythmias. Each chapter is accompanied by illustrative electrocardiograms and, where thought to be useful, practical algorithms that help
delineate an organized approach to arrhythmia diagnosis and management.
This is the first practical handbook written on this topic that is aimed at practicing clinicians
of all specialties, that is based on a contemporary approach, and that focuses on new and
advanced therapeutic options and technologies. We believe that the reader will refer to this
book often and find it to be compelling, concise, comprehensive, and relevant. It is hoped that
this book will find its way to a lab coat pocket and be available on patient care units rather
than sit on the library bookshelf.

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Arrhythmia Essentials
ABBREVIATIONS

1° AVB
2° AVB
3° AVB
AAT
AED
AF
AFL
AIVR
ART
ARVC

first-degree atrioventricular block
second-degree atrioventricular block
third-degree atrioventricular block
automatic atrial tachycardia
automatic external defibrillator
atrial fibrillation
atrial flutter
accelerated idioventricular rhythm
atrial reentrant tachycardia
arrhythmogenic right ventricular
cardiomyopathy
AT
atrial tachycardia
ATP
antitachycardia pacing
AV
atrioventricular
AVB (or AV atrioventricular block

Block)
AVNRT
atrioventricular node reentry
tachycardia
AIVR
accelerated idioventricular rhythm
AVRT
atrioventricular reentry tachycardia
BBB
bundle branch block
BBRVT
bundle branch reentrant ventricular
tachycardia
BP
blood pressure
bpm
beats per minute
CABG
coronary artery bypass graft
CAD
coronary artery disease
CHB
complete heart block
CHF
congestive heart failure
COPD
chronic obstructive pulmonary
disease
CPVT
catecholaminergic polymorphic

ventricular tachycardia
CRT
cardiac resynchronization therapy
CSM
carotid sinus massage
DAD
delayed afterdepolarizations
EAD
early afterdepolarizations
EAR
ectopic atrial rhythm
ECG
electrocardiogram
EP
electropyhsiology
EPS
electrophysiology study
HCM
hypertrophic cardiomyopathy
ICD
implantable cardioverter defibrillator

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ILR
ILVT

implantable loop recorder
idiopathic left ventricular
tachycardia

INR
international normalized ratio
IST
inappropriate ST
JT
junctional tachycardia
LAFB
left anterior fascicular block
LBB
left bundle branch
LBBB
left bundle branch block
LPFB
left posterior fascicular block
LQTS
long QT interval syndrome
LV
left ventricle
LVEF (or EF) left ventricular ejection fraction
LVH
left ventricular hypertrophy
MAO
monoamine oxidase
MAT
multifocal atrial tachycardia
MI
myocardial infarction
MVP
mitral valve prolapse
NSR

normal sinus rhythm
NSVT
nonsustained ventricular
tachycardia
NYHA
New York Heart Association
PAC
premature atrial contractions
PAD
premature atrial depolarization
PJC
premature junctional complex
PJRT
permanent junctional reentrant
tachycardia
PM
pacemaker
PMT
pacemaker-mediated tachycardia
POTS
postural orthostatic tachycardia
syndrome
PRN
pro rata nata (as needed)
PT
prothrombin time
PTT
partial thromboplastin time
PVARP
postventricular atrial refractory

period
PVC
premature ventricular contraction
RBB
right bundle branch
RBBB
right bundle branch block
RV
right ventricle
RVOT
right ventricular outflow tract
SA
sinoatrial
SB
sinus bradycardia

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Abbreviations
SND
SNRT
SVT
TdP
TEE
TIA

sinus node dysfunction
sinus node reentry tachycardia
supraventricular tachycardia

torsades de pointes
transesophageal echocardiogram
transient ischemic attack

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TTE
VF
VT
WAP
WCT
WPW

vii
transthoracic echocardiogram
ventricular fibrillation
ventricular tachycardia
wandering atrial pacemaker
wide complex tachycardia
Wolff-Parkinson-White

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Chapter 1. Sinus Node—Normal and Abnormal Rhythms

1

Chapter 1
Sinus Node—Normal and Abnormal Rhythms
Normal Sinus Node . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sinus Node Dysfunction, Including Sinus Bradycardia and Tachy-Brady Syndrome . .
Sinoatrial Exit Block . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sinus Pause/Arrest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sinus Tachycardia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Postural Orthostatic Tachycardia Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

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2
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13
18
20
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NORMAL SINUS NODE

Description

A normal sinus rhythm (NSR) is an atrial rhythm caused by electrical activation that originates
from the sinus node, a structure located in the area of the junction of the right atrium and
superior vena cava. NSR P waves, representing atrial depolarization (but not sinus node activity
itself), are upright in leads I and aVL and the inferior leads (II, III, aVF), indicating the high to
low atrial activation pattern (Figure 1.1). The P wave in leads V1–V2 may be upright, biphasic,
or slightly inverted, whereas the P waves in leads V3–V6 tend to be upright, indicating right to
left atrial activation. The P-wave morphology may change with alterations in autonomic tone,
heart rate, and atrial abnormalities such as hypertrophy. High vagal tone can be associated with
a more inferior exit of the impulse from the sinus node, whereas high sympathetic tone can be
associated with a more superior exit from the node.

Clinical Symptoms and Presentations
NSR is generally considered to have a rate of 60 to 100 beats per minute (bpm), although
50 bpm is still normal. Rate changes with alterations in autonomic tone; at rest, most
individuals have their heart rate regulated by the vagus nerve.
Individuals with high vagal tone (such as those who are in excellent physical condition)
may exhibit sinus arrhythmia, a normal rhythm, in which the rate varies with respiration
(Figure 1.2). In sinus arrhythmia, inspiration increases the rate and expiration decreases the
rate. Sinus arrhythmia is common during sleep and in patients with obstructive sleep apnea,
in which the decrease in rate can be substantial.
Various forms of sinus arrhythmia exist, including a non–respiration-dependent form that
may indicate sinus node dysfunction (SND).
Ventriculophasic sinus arrhythmia is present when alterations in the sinus rate are due
to atrioventricular (AV) block: The P-P intervals enclosing a QRS complex are shorter than P-P
intervals not enclosing a QRS complex.
A change in sinus rate can be gradual or abrupt and can occur with change in body
position and exercise. Patients who are in good physical condition generally have more
gradual acceleration in sinus rate with exercise and a rapid slowing of the sinus rate at
the end of exercise compared with less physically fit individuals or individuals with heart
disease. Higher resting sinus rates have been associated with increased risk for overall

mortality.

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aVL

aVF

II

III
V3

V2

V1

V6

V5

V4

Normal sinus rhythm is characterized by P waves that are usually upright in leads I, aVL, II, III, aVF, and V3–V6 at a rate between 60 and 100 beats/min
(bpm).

Figure 1.1. Normal Sinus Rhythm

V5

II

VI

aVR

I

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Arrhythmia Essentials

Figure 1.2. Normal Sinus Rhythm with Sinus Arrhythmia
This lead II rhythm strip shows normal sinus rhythm with sinus arrhythmia, in which the P-P intervals vary
by > 0.16 seconds. Sinus arrhythmia is often related to respiratory cycles.

Wandering atrial pacemaker (WAP) (Figure 1.3) occurs in association with higher vagal
tone and is a benign rhythm. In wandering atrial pacemaker, there are varying exit points of
the sinus impulse from the sinus node or impulses that originate from the sinus node and

wander from the node to the low atrium and back. Wandering atrial pacemaker is often seen
in patients with sinus arrhythmia. Wandering atrial pacemaker should not be confused with
“multifocal atrial rhythm” (Figure 3.13).

Approach to Management
Although sinus rhythm generally does not require any treatment, an inability to increase the
sinus rate in response to increases in metabolic needs (“chronotropic incompetence”) may
require permanent cardiac pacing when it is documented to cause symptoms. Definitions of
chronotropic incompetence are many and varied, and there is no general agreement as to
its parameters.

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aVF

III

V6

V5

V4

This 12-lead ECG II rhythm strip shows wandering atrial pacemaker. There is a low atrial rhythm with inverted P waves in lead II (2nd through 4th beats)
that changes to sinus rhythm (6th through 12th beats) in a phasic manner. The 5th QRS complex is preceded by a P wave with a morphology that is

intermediate in morphology between the sinus and the other atrial pacemaker, and likely represents atrial fusion, in which the atria are depolarized
from two sources.

Figure 1.3. Wandering Atrial Pacemaker

II

V2

aVL

II

V3

V1

aVR

I

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SINUS NODE DYSFUNCTION, INCLUDING SINUS BRADYCARDIA AND
TACHY-BRADY SYNDROME

Description
Sinus bradycardia (SB) (Figure 1.4) is generally defined as sinus rates of < 60 bpm, although
50 bpm is likely within the normal range of rate. SB is often a normal finding in young, healthy
adults, especially in athletes with high vagal tone. SB frequently occurs at rest and during
sleep. In trained athletes or individuals with high vagal tone, sinus rates in the 40s and even
at times in the 30s, especially during sleep, are not uncommon. SB may be associated with a
narrow QRS complex or, in the presence of bundle branch block or intraventricular conduction
delay, with a wide QRS complex (Figure 1.5).

II
Figure 1.4. Sinus Bradycardia
This lead II rhythm strip shows sinus bradycardia, which is characterized by sinus P waves (usually upright in
leads II, III, aVF) with rate < 60 bpm.

The sinus rate normally slows with age. SND from sinus node degeneration is more
frequent in older persons. SND, sometimes termed “sick sinus syndrome,” is a very common
arrhythmia and includes sinus pauses, sinus arrest, inappropriate SB, chronotropic incompetence, sinoatrial (SA) exit block, combinations of SA and AV conduction abnormalities, and
tachycardia-bradycardia (tachy-brady) syndrome (e.g., paroxysmal or persistent atrial tachyarrhythmias with periods of bradyarrhythmia [Figure 1.6] or postconversion sinus pauses).

Associated Conditions
SB is often associated with sinus arrhythmia, escape rhythms (junctional and ventricular),
accelerated (junctional and ventricular) rhythms, atrial arrhythmias, wandering atrial pacemaker, or SA or AV Wenckebach-like periods. SB is usually benign but can be associated with
certain conditions and diseases, including hypothyroidism, vagal stimulation, carotid sinus
hypersensitivity, increased intracranial pressure, myocardial infarction, and drugs such as
beta-adrenergic (β-adrenergic) blockers (including those used for glaucoma), calcium channel
blockers, amiodarone, sotalol, clonidine, lithium, and parasympathomimetic drugs. SB occurs
in 14% to 36% of myocardial infarctions and can be associated with AV block. The bradycardia usually resolves without the need for chronic therapy. SB is usually associated with

inferior–posterior infarction (caused by increased vagal tone from stimulation of vagal
afferents, the Bezold-Jarisch reflex). Clinical syndromes, such as neurocardiogenic syncope
and some specific rhythm disorders such as the tachy-brady syndrome, can be associated

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Although the QRS complex is normally narrow (< 0.12 sec), the QRS can be wide in the setting of bundle branch block or intraventricular conduction
delay. This 12-lead ECG with rhythm strips of leads V1, II, and V5 shows sinus bradycardia (rate 46 bpm) with first-degree AV block and left bundle branch
block with left axis deviation.

Figure 1.5. Sinus Bradycardia with Wide QRS Complex

V5

II

V1

aVF

III

V6

V5

V2

aVL

II

V3

V4

V1

aVR

I

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Arrhythmia Essentials
N

N

N

N

V

N

Figure 1.6. Tachy-Brady Syndrome
This rhythm strip tracing shows a supraventricular tachycardia (SVT) with preceding P waves (consistent
with atrial tachycardia) that suddenly terminates. The SVT is followed by a 4.2-second pause and then a
junctional escape beat, a spontaneous P wave with aberrant conduction and a sinus beat. The combination
of a tachycardia that is suddenly followed by a bradycardia is characteristic of tachy-brady syndrome.

with symptomatic bradycardia as well as symptoms caused by rapid ventricular rates during
atrial fibrillation or flutter; severe SB or sinus arrest can occur after spontaneous conversion
prior to recovery of the sinus node. SB can be exacerbated by drugs that are used to slow AV
node conduction during atrial arrhythmias.

Clinical Symptoms and Presentation
SB is asymptomatic in the vast majority of patients. When present, symptoms may include
fatigue, effort intolerance, palpitations, dizziness, lightheadedness, near-syncope, syncope,
dyspnea, and angina. SND, including chronotropic incompetence, can impair cardiac output
or exacerbate heart failure and can be associated with or trigger atrial arrhythmias (e.g.,
atrial fibrillation) and ventricular arrhythmias (e.g., torsades de pointes). Hemodynamic tolerance of SB is a function of heart rate (a rate of < 30 bpm is usually not well tolerated),
underlying disease (less well tolerated with poor ventricular function), and age (better tolerated in those < 50 years old). Tachy-brady syndrome may present with rapid palpitations
during atrial arrhythmias and lightheadedness, dizziness, near syncope, and/or syncope
during postconversion pauses. SND and/or tachy-brady syndrome can result from cardiac
surgery, particularly associated with right atriotomy. SND is relatively common after heart
transplantation, as the donor atria can be damaged by ischemia and by atrial anastomoses.

The sinus node of the native heart rarely interacts with or affects the transplanted sinus rate.
Other causes of SB and/or pauses in heart transplant patients include drugs (rare), trauma,
and rejection.

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9

Approach to Management
Evaluation or treatment often is unnecessary if the patient is asymptomatic. Treatment
depends on the nature of the rhythm disturbance and is usually directed toward prevention
of symptoms. Asystole can be life threatening, but more often it causes symptoms and is
due to vagal surges or SND. Asystolic pauses in a young, otherwise healthy person are generally due to vagal surges related to a neurocardiogenic response. An asystolic response after
cardioversion, after a tachycardia, and in a patient who is older or has heart disease is often
due to SND. Because SND can be subclinical but exacerbated by medical therapy, rate-slowing
drugs should be avoided if possible.
A heart rate < 30 bpm is an indication to evaluate further for treatment. Symptoms
caused by SND can be difficult to assess. Exercise testing (if feasible with a temporary pacemaker if a previous exercise test showed inappropriate heart rate response) can help distinguish the cause of symptoms. If severe SND (i.e., SB associated with sinus exit block, sinus
pauses, and sinus arrest) is suspected but cannot be documented by physical examination,
telemetry monitor strip, or electrocardiogram (ECG), it can be evaluated further with a Holter
monitor (low sensitivity), event monitor, implantable loop recorder, or electrophysiology test
(low sensitivity and specificity).
The timing of the pauses or the bradycardia is important. It is not uncommon for
a patient to develop SB or asystolic episodes during sleep. Although often caused by
enhanced vagal tone, this may in some patients be related to sleep apnea. If pauses are

seen during sleep on telemetry or Holter monitoring, sleep apnea should be considered
and ruled out.
Short-term monitoring is used for the acute setting in the hospital. Such monitoring is
capable of detecting all rhythm disturbances over a period of time. Admitting a patient with
symptoms suggestive of bradycardia and then placing the patient on a monitor are usually
unproductive steps unless the patient is having frequent and severe episodes. Thus, the firstline approach is long-term monitoring, as long as this approach is considered safe. External
event recorders can document episodes of symptomatic SB, but their yield will depend on
the frequency of the episodes. In some instances, these events can be difficult to capture
because of their episodic nature; in these cases, an implantable loop recorder that continuously records and erases the cardiac rhythm, but has memory, may be optimal. This leadless
implant can record and save episodes automatically or can be triggered manually.
The Holter monitor, a continuous 24-hour ambulatory monitor, has the advantage of
determining all heart rhythms, symptomatic or asymptomatic, and therefore helps to determine the presence or absence of sinus node disease; however, correlative information
between rhythm and symptoms is often lacking.
Electrophysiology testing can be used to determine SND. The test includes a measurement
for sinoatrial conduction time and sinus node recovery time. Both of these measurements
have a low degree of sensitivity, and the specificity is essentially unknown. Thus, the utility
of the electrophysiology test is relatively uncertain and is not a test that is used routinely to
diagnose or exclude the arrhythmia.

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Autonomic testing is generally not performed to determine the effect of parasympathetic and sympathetic activation as a cause for changes in heart rate. In patients with
syncope in whom a neurocardiogenic reflex is suspected but not diagnosed with certainty,

the tilt table test may be helpful in determining its presence. The tilt-table test has an
unclear specificity and sensitivity, and there is no gold standard to determine the presence
or absence of the neurocardiogenic reflex and the relationship of this reflex to SB or
asystole. The accuracy with which this test predicts the cause of syncope is dependent on
both the protocol and the patient. In a patient with apparent asystolic episodes caused
by suspected SND, the tilt table test may be helpful in distinguishing an autonomic reflex
from SND.
For the patient with recent syncope or severe symptoms thought to be due to SND, hospital admission is required, especially for those with multiple medical problems, those who
have been injured, and those who are older. Acute treatment is needed if there are severe
symptoms or serious sequelae of bradycardia (Table 1.1).
Permanent cardiac pacing is the treatment of choice for symptomatic SB (including
chronotropic incompetence) if there is no transient (such as vasovagal bradycardia) or
reversible cause or if the SB occurs as a result of essential drug therapy. Patients with
tachy-brady syndrome may require permanent pacing to facilitate drug treatment of
their atrial arrhythmias, as drug therapy for rapid atrial arrhythmias may aggravate the
bradyarrhythmias.
Pacing may be indicated for specific patients in whom the relationship between the bradycardia and hemodynamic compromise can be demonstrated.
After cardiac surgery, sinus node function that fails to recover may also necessitate a
permanent pacemaker. Because it can take 5 to 6 weeks before full return of sinus node function, frequently a decision is made to implant a pacemaker by the fifth to seventh post-op day
before hospital discharge. It is best to make that decision while temporary pacing wires are
still in place so that temporary pacing can be instituted if it is necessary.
Table 1.1. Sinus Node Dysfunction and Sinus Bradycardia Management
Setting
Asymptomatic

Therapy
•

•
•

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No therapy required. There is some relationship between the presence of
sleep apnea and sinus node dysfunction; some reports have suggested
that permanent pacing, even in asymptomatic patients, may benefit sleep
apnea.
Identify and treat associated medical conditions such as
hypothyroidism.
Avoid rate-slowing drug if feasible.

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Chapter 1. Sinus Node—Normal and Abnormal Rhythms

11

Table 1.1. Sinus Node Dysfunction and Sinus Bradycardia Management (cont’d)
Setting
Symptomatic–
Acute

Therapy
•

•

•

•

•

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Treat reversible causes. Consider drugs as the cause (β-adrenergic
blockers, calcium channel blockers, and digoxin, antiarrhythmic drugs
[sotalol, amiodarone, flecainide, and propafenone]). A drug may be a
contributor, but until the problem resolves, treatment will be required.
Atropine 0.6–2 mg IV every 5 minutes up to a total of 2 mg. Low doses
and slow infusion may cause paradoxical bradycardia due to increase
in sinus rate and degree of AV block. Atropine will not work for heart
transplant patients. This is only a short-term solution.
Isoproterenol 1–5 mcg/min is effective but can exacerbate myocardial
ischemia. Do not give in patients with unstable coronary artery disease.
Isoproterenol is rarely indicated and should only be considered in
extreme conditions when a temporary pacemaker is not available.
Temporary pacemaker (preferably atrial, if AV conduction is intact and
the bradycardia is not due to high vagal tone) if unstable and episodes
are prolonged, persistent, highly symptomatic, recurrent, or unresponsive
to acute medical therapy, such as atropine or isoproterenol, or with
bradycardia-associated ventricular arrhythmias (e.g., torsades de pointes).
Temporary pacing may be used if permanent pacing is not possible, not
indicated, or dangerous (such as the presence of an ongoing infection).
Temporary pacing can be accomplished by epicardial wires (after
cardiovascular surgery) or by temporary balloon-tipped catheters placed
percutaneously with or without fluoroscopy (unreliable) or a temporary
bipolar lead (screw in or not) that is more reliable. Placement of a
temporary pacemaker can be associated with adverse events.

It should be undertaken only if there is a long-term need to pace, but
there is no immediate permanent pacemaker placement availability
(e.g., patients with recurrent syncope who on monitoring have pauses
of 5 seconds or more, symptomatic or not). Temporary pacing is not
indicated if there are prolonged pauses caused by neurocardiogenic
reasons (e.g., vasovagal syncope, suctioning, endoscopy, vomiting,
and cough).
Transcutaneous pacing may be used emergently prior to placement of
a temporary pacing lead. It is highly unreliable and painful. It is not very
effective over time and is hardly ever indicated. It could be used for a
patient who has precipitous hemodynamic collapse due to persistent or
recurrent asystole. It has not been shown to reduce the risk of death
but occasionally can be used until an adequate temporary pacemaker is
placed. Most patients with episodic asystole do not fit into the category
of having a life-threatening arrhythmia, but patients with prolonged and
recurrent asystole might fit into this category, especially if the patient
is older and had underlying heart disease. Transcutaneous pacing is
not stable over time because of impedance changes between the large
electrodes and myocardium; moreover, adequate sedation is usually
necessary to prevent pain.

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Arrhythmia Essentials

Table 1.1. Sinus Node Dysfunction and Sinus Bradycardia Management (cont’d)
Setting

Therapy

Symptomatic–
Chronic

•

Permanent pacemaker Class I (ACC/AHA recommended) indications:
Documented symptomatic SB, including frequent pauses that cause
symptoms; symptomatic bradycardia occurring as a consequence of
essential long-term drug therapy at a dose and type for which there are
no acceptable alternatives; symptomatic chronotropic incompetence.
Class IIa (ACC/AHA accepted, not mandatory, well substantiated)
indications: Sinus node dysfunction from necessary drug therapy with
HR < 40 bpm when a clear association between presence of bradycardia
and significant symptoms has not been documented; syncope of
undetermined origin with major abnormalities in sinus node dysfunction
found at electrophysiology (EP) study. Class IIb (ACC/AHA accepted, not
mandatory, less well substantiated): Minimally symptomatic patients with
chronic awake HR < 40 bpm.
Temporary transvenous pacemaker, if severe symptoms associated with
HR < 30 bpm, unresponsive to acute medical therapy (e.g., atropine,
isoproterenol) or bradycardia-associated ventricular arrhythmias (e.g.,
torsades de pointes). Temporary pacing is rarely indicated for chronic
symptomatic problems unless there are frequent recurrences of
symptomatic pauses or bradycardia.

•

Table 1.2. Sinus Node Dysfunction Management in Specific Clinical Circumstances
Setting
Myocardial
infarction (MI)

Therapy
•

•

•

Common causes for SB in setting of an acute MI: β-adrenergic blockers,
calcium channel blockers, amiodarone, morphine, lidocaine, chronic
antiarrhythmic drugs, pain, increased vagal tone (especially with inferior
MI), atrial ischemia. Usually resolves.
In addition to symptomatic SB, additional indications for treatment of SB
include recurrent or worsening ischemia (evident by ST segment changes
on the ECG), poor cardiac output, hypotension, or bradycardia-related
ventricular arrhythmias. These are more common in the first 3 to 5 days
after infarction.
Temporary pacing if there is symptomatic SB (despite stopping
medications, including β-adrenergic blockers), prolonged pauses
(> 3 seconds recurrently or occasional ones > 5 seconds), hypotension,
heart failure symptoms. Permanent pacing is rarely needed. In some
instances, a wait of 5 to 7 days may not be long enough to know if
there is complete resolution of bradycardia. In that case, a permanent
pacemaker is indicated when there are continued pauses or heart
rates < 40 per minute. Treadmill exercise testing can be used to
ascertain chronotropic competence after MI.

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Chapter 1. Sinus Node—Normal and Abnormal Rhythms

13

Table 1.2. Sinus Node Dysfunction Management in Specific Clinical Circumstances
(cont’d)
Setting
Pre-op

Therapy
•
•
•

Post-op

•
•

Heart
transplant

•
•

•
•

Atropine should be available, especially at induction of anesthesia and
during intubation when vagal tone is high.
SB is very common intraoperatively due to maneuvers that increase vagal
tone such as intubation. If hypothermia is planned, SB can be expected.
No treatment is required.
Even if asymptomatic, patients who cannot increase cardiac output
because of SB may require temporary pacing.
SB is common, often due to pain, opiates, or effect of surgery itself, and is
usually not treated.
Temporary pacing (preferably atrial but with ventricular backup pacing
if there is a vagal component) at 80 to 100 bpm can be used in cases of
hemodynamic decompensation. Permanent pacing should be considered if
SB does not resolve after 3 to 5 post-op days.
One to three weeks after transplant, SND, including SB, may resolve and
need no chronic therapy.
Acutely, isoproterenol is first-line therapy, as opposed to atropine, which
will not work in the denervated heart.
Theophylline 150 to 200 mg po bid may work in the subacute setting.
Although effective in the short term, it has not been shown to be effective
over the long term.
After 10 to 20 days, if persistent, symptomatic, and not expected to resolve,
SND may require treatment with a permanent pacemaker. An atrial pacing
device might be considered to avoid tricuspid valve damage (patient may need
repeated biopsies that may dislodge pacing leads), but make sure it is secure in
the transplanted donor (not recipient) atrium, such that paced atrial beats will
conduct intrinsically to the ventricles.

SINOATRIAL EXIT BLOCK

Description
SA exit block results from a block in conduction from the sinus node to the atria. It usually
appears on the ECG as the absence of a P wave, with the pause duration being a multiple of the
basic P-P interval. In first-degree SA block, conduction of sinus impulses to the atrium is delayed,
but a 1:1 response is maintained; because impulse formation in the sinus node is not visible on
the ECG, it is impossible to diagnose as it looks like sinus rhythm. Second-degree SA block takes

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Arrhythmia Essentials

the form of type I or type II (analogous to AV block); some sinus impulses fail to depolarize the
atria (i.e., intermittent absence of a P wave). Type I (Wenckebach pattern) SA block (Figure 1.7)
is characterized by normal P-wave morphology and axis consistent with a sinus node origin and
group beating with (1) progressive shortening of the P-P interval leading up to a pause in P-wave
rate, (2) constant PR interval, and (3) P-P pauses < twice the normal P-P interval.
Type II SA block (Figure 1.8) is characterized by a constant P-P interval followed by a
pause that is a multiple (e.g., 2×, 3×) of the normal P-P interval. The pause may be slightly <
twice the normal P-P interval but is usually within 0.10 seconds of this interval. Third-degree
SA block indicates complete failure of SA conduction but cannot be differentiated from a
sinus pause (see Sinus Pause, p. 18).

Associated Conditions

SA exit block is usually related to drug therapy (digoxin, calcium channel blockers, β-adrenergic
blockers), vagal stimulation, SND with degenerative disease of the sinus node and atrium, or
hyperkalemia. It is unusual after myocardial infarction (MI) but may be caused by vagal excess
(Bezold-Jarisch reflex) from an inferoposterior MI. If unrelated to an acute cause that is reversible or transient, SA exit block may cause progressive bradycardia.

Clinical Symptoms and Presentation
SA exit block may be asymptomatic or associated with mild palpitations because of pauses
and the irregularity of heart rate; however, most symptoms are similar to those listed under
SB (p. 8).

Approach to Management
Patients should be assessed for potentially reversible causes (e.g., drugs) and then monitored, and any inciting stimulus should be removed. If asymptomatic, no therapy is indicated,
although close follow-up for progressive bradycardia should be maintained. Treatment is indicated only if symptomatic and involves the avoidance of precipitating factors and possibly
atrial pacing for persistent symptoms.

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This is a rhythm strip of leads V1 and II showing sinus rhythm (rate 77 bpm) with sinus pauses that are twice the prevailing P-P interval.

Figure 1.8. Sinoatrial Exit Block Type II

V1

This is a lead II rhythm strip of sinus rhythm (rate ~75 bpm) with a recurring pattern of group beating in which two normally conducted P waves
(with the same morphology) are followed by a pause < twice the prevailing P-P interval. This represents 3:2 SA exit block (type I) in a patient that

has sinus node dysfunction.

Figure 1.7. Sinoatrial Exit Block Type I

II

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Arrhythmia Essentials

Table 1.3. Sinoatrial Exit Block and Sinus Pause Management
Setting
Type I or II
second-degree
block

Therapy
•
•
•
•

MI

•

•
Pre-op

•
•
•
•

Post-op

•

74769_CH01_Printer.indd 16

If asymptomatic: no therapy.
If symptomatic bradycardia: acutely—atropine; chronically (rare)—
permanent Single Chamber Rate Adaptive Pacemaker or Dual Chamber
Rate Adaptive Pacemaker cardiac pacing (see SB, p. 6).
Discontinue responsible drugs (e.g., digoxin), if possible. If not possible,
and there are episodes of symptomatic bradycardia, a permanent
pacemaker is indicated.
Exclude hyperkalemia.
If symptomatic bradycardia: acutely—atropine; note, however,
that atropine can occasionally produce increased sinus node firing
rate, increased SA exit block, and paradoxical slowing of atrial and
ventricular rate.
Usually transient. External pacing if pauses are prolonged and cause
hemodynamic embarrassment.

If asymptomatic: no specific therapy. External pacer available.
If elective surgery and symptomatic with no reversible cause: atrial or
dual chamber [AAI(R) or DDD(R)] pacemaker before surgery.
If urgent surgery and symptomatic: atropine and assure availability of a
temporary external or transvenous endocardial pacemaker.
Vagal stimulation due to intubation, Foley catheter placement, and so
forth may worsen block but may respond well to atropine.
Usually no treatment but pace temporarily if symptomatic or
hypotensive.

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